This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.

OTI Disclaimer:

Due to the inherent nature of this plasmid, standard methods to replicate additional amounts of DNA in E. coli are highly likely to result in mutations and/or rearrangements. Therefore, OriGene does not guarantee the capability to replicate this plasmid DNA. Additional amounts of DNA can be purchased from OriGene with batch-specific, full-sequence verification at a reduced cost. Please contact our customer care team at custsupport@origene.com or by calling 301.340.3188 option 3 for pricing and delivery.

The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info

The Reference Sequence (RefSeq) collection provides a comprehensive, integrated, non-redundant set of sequences. This database is built by NCBI, and, provides only a single record for each gene/transcript. More details.
Due to SNPs, each gene/transcript has many variations in the sequence; those variations are naturally occurring. Therefore, Refseq is one curated sequence, not to be perceived as the wild type.

Synonyms: CADASIL; CADASIL1; CASIL; IMF2; LMNS

RefSeq Size: 6963

RefSeq ORF: 6966

LocusID: 4854

Cytogenetic: 19p13.12

Domains: NL, EGF_CA, ANK, EGF, EGF

Gene Summary: This gene encodes the third discovered human homologue of the Drosophilia melanogaster type I membrane protein notch. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signalling pathway that plays a key role in neural development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remains to be determined. Mutations in NOTCH3 have been identified as the underlying cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). [provided by RefSeq, Jul 2008].